Research article

Dynamics and density function of a HTLV-1 model with latent infection and Ornstein-Uhlenbeck process

  • Received: 17 September 2024 Revised: 25 November 2024 Accepted: 04 December 2024 Published: 31 December 2024
  • MSC : 60H10, 37A50

  • This paper examines the propagation dynamics of a T-lymphoblastic leukemia virus type Ⅰ (HTLV-1) infection model in a stochastic environment combined with an Ornstein-Uhlenbeck process. In conjunction with the theory of Lyapunov functions, we initially demonstrate the existence of a unique global solution to the model when initial values are positive. Subsequently, we establish a sufficient condition for the existence of a stochastic model stationary distribution. Based on this condition, the local probability density function expression of the model near the quasi-equilibrium point is solved by combining it with the Fokker-Planck equation. Subsequently, we delineate the pivotal conditions that precipitate the extinction of the disease. Finally, we select suitable data for numerical simulation intending to corroborate the theorem previously established.

    Citation: Yan Ren, Yan Cheng, Yuzhen Chai, Ping Guo. Dynamics and density function of a HTLV-1 model with latent infection and Ornstein-Uhlenbeck process[J]. AIMS Mathematics, 2024, 9(12): 36444-36469. doi: 10.3934/math.20241728

    Related Papers:

  • This paper examines the propagation dynamics of a T-lymphoblastic leukemia virus type Ⅰ (HTLV-1) infection model in a stochastic environment combined with an Ornstein-Uhlenbeck process. In conjunction with the theory of Lyapunov functions, we initially demonstrate the existence of a unique global solution to the model when initial values are positive. Subsequently, we establish a sufficient condition for the existence of a stochastic model stationary distribution. Based on this condition, the local probability density function expression of the model near the quasi-equilibrium point is solved by combining it with the Fokker-Planck equation. Subsequently, we delineate the pivotal conditions that precipitate the extinction of the disease. Finally, we select suitable data for numerical simulation intending to corroborate the theorem previously established.



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